title: Cystometric parameters and the activity of signaling proteins in association with the compensation or decompensation of bladder function in an animal experimental model of partial bladder outlet obstruction.
abstract: We conducted this study to determine whether the degree of detrusor contractility is associated with the compensation or decompensation of bladder function depending on the residual volume (RV) during the first two weeks after the onset of partial bladder outlet obstruction (BOO). Moreover, we also examined whether the degree of the phosphorylation and expression of signaling proteins [AMP-activated kinase (AMPK), extracellular signal‑regulated protein kinases 1 and 2 (ERK1/2) and protein kinase C (PKC)] is associated with the prevalence of compensation or decompensation of bladder function. Twenty-seven female Sprague-Dawley (SD) rats were randomly assigned to either the sham-operated group (n=7) or the group with partial bladder outlet obstruction (BOO) (n=20). We then measured cystometric parameters from three reproducible micturition cycles and averaged the results for a comparison between the two groups. Based on a cut-off value of a mean RV% of 25%, we subdivided our experimental animals into two subgroups: the subgroup with bladder compensation (mean RV%, <25%) and the subgroup with bladder decompensation (mean RV%, >25%). Our results indicated that the degree of detrusor overactivity (DO) was associated with the compensation or decompensation of bladder function depending on the RV during the first two weeks after the onset of BOO in an animal experimental model of partial BOO. Moreover, we also demonstrate that AMPK and ERK1/2 are involved in the compensation or decompensation of bladder function. Furthermore, our results suggest that PKC is not involved in two-phase bladder contraction. Alterations in the activities of signaling proteins, such as AMPK and ERK1/2 may prove to be helpful in the treatment of patients with voiding difficulty.
authors.affiliation: Department of Pharmacology, Inha University College of Medicine by BK 21 Project, Incheon, Republic of Korea.
authors.forename: Bo-Hwa
authors.initials: BH
authors.lastname: Choi
authors.forename: Long-Hu
authors.initials: LH
authors.lastname: Jin
authors.forename: Khae-Hawn
authors.initials: KH
authors.lastname: Kim
authors.forename: Sung-An
authors.initials: SA
authors.lastname: Kang
authors.forename: Ju-Hee
authors.initials: JH
authors.lastname: Kang
authors.forename: Sang-Min
authors.initials: SM
authors.lastname: Yoon
authors.forename: Chang-Shin
authors.initials: CS
authors.lastname: Park
authors.forename: Tack
authors.initials: T
authors.lastname: Lee
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D009130:Muscle, Smooth / Q000378:metabolism / Q000503:physiopathology; D010766:Phosphorylation; D011312:Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D001743:Urinary Bladder / Q000378:metabolism* / Q000503:physiopathology*; D001748:Urinary Bladder Neck Obstruction / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology*; D053201:Urinary Bladder, Overactive / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D014572:Urology / Q000379:methods*